Congenital deafness and sinoatrial node dysfunction in mice lacking class D L-type Ca2+ channels.

By J. Platzer, J. Engel, A. Schrott-Fischer, Kurt Stephan, S. Bova, Howard Y. Chen, Hui Zheng, J. Striessnig. Cell, 2000

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Regulation of Cardiac L-Type Calcium Channels by Protein Kinase A and Protein Kinase C (2000, background): “3).(18,19) In vivo, a substantial portion of a1C undergoes proteolytic processing about 400 to 500 residues away from”
The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential (2015, background): “3 is also the prominent L-type channel in AVN cells and contributes to AVN conduction and pacemaking (Platzer et al., 2000; Marger et al., 2011b).”
Neuronal voltage-gated calcium channels: structure, function, and dysfunction. (2014, background): “3 are deaf (Platzer et al., 2000), as this channel subtype is critical for auditory hair cell synaptic transmission.”
Selective elimination of glutamatergic synapses on striatopallidal neurons in Parkinson disease models (2006, methodology): “3α1 subunits has long-term effects on spine morphology or number, two-photon laser scanning microscopy (2PLSM) was used to visualize spines in MSNs from wild-type and Cacna1d −/− mic”
Voltage-gated calcium channels. (2011, positive): “3 channels causes deafness in mice (Platzer et al. 2000).”
Cav1.3 (α1D) Ca2+ Currents in Neonatal Outer Hair Cells of Mice (2003, methodology): “3 channels are expressed in a variety of neurons, neuroendocrine, endocrine, cardiac pacemaker and sensory cells (Hell et al. 1993; Ihara et al. 1995; Platzer et al. 2000; Zhang et al. 2002; Mangoni et al. 2003).”